Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cancer cachexia.

Michael J Tisdale1

  • 1Pharmaceutical Sciences Research Institute, Aston University, B4 7ET, Birmingham, UK. m.j.tisdale@aston.ac.uk

Langenbeck'S Archives of Surgery
|May 29, 2004
PubMed
Summary
This summary is machine-generated.

Cancer cachexia causes muscle and fat wasting through increased protein breakdown and lipolysis, driven by tumor and host factors. Eicosapentaenoic acid (EPA) can prevent muscle wasting and promote lean mass gain in cachectic patients.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Simple ammonium salts acting on sigma-1 receptors yield potential treatments for cancer and depression.

Scientific reports·2020
Same author

Ken Fearon.

Cell metabolism·2016
Same author

In vitro assessment of the combined effect of eicosapentaenoic acid, green tea extract and curcumin C3 on protein loss in C2C12 myotubes.

In vitro cellular & developmental biology. Animal·2016
Same author

Comparison of the anticatabolic effects of leucine and Ca-β-hydroxy-β-methylbutyrate in experimental models of cancer cachexia.

Nutrition (Burbank, Los Angeles County, Calif.)·2014
Same author

Attenuation of muscle wasting in murine C2C 12 myotubes by epigallocatechin-3-gallate.

Journal of cachexia, sarcopenia and muscle·2014
Same author

Role of β-adrenergic receptors in the oral activity of zinc-α2-glycoprotein (ZAG).

Endocrinology·2012

Area of Science:

  • Oncology
  • Metabolism
  • Biochemistry

Background:

  • Cancer cachexia involves muscle atrophy and fat loss, unresponsive to nutritional support alone.
  • Tumor and host factors, including proteolysis-inducing factor (PIF) and tumor necrosis factor-alpha (TNF-alpha), drive catabolic processes.
  • Increased lipolysis, not decreased synthesis, characterizes adipose tissue loss in cancer patients.

Purpose of the Study:

  • To investigate the causative factors of muscle atrophy and adipose tissue loss in cancer cachexia.
  • To evaluate the efficacy of eicosapentaenoic acid (EPA) in managing cancer cachexia.

Main Methods:

  • Analysis of protein synthesis and degradation pathways, including the ubiquitin-proteasome system.
  • Measurement of mRNA levels for key lipolytic enzymes like hormone-sensitive lipase (HSL).

Related Experiment Videos

  • Clinical assessment of EPA's effects on body composition and muscle wasting in cachectic patients.
  • Main Results:

    • Increased ubiquitin-proteasome pathway activity contributes to myofibrillar protein degradation.
    • Tumor necrosis factor-alpha (TNF-alpha) and lipid-mobilising factor (LMF) increase lipolysis via cyclic AMP activation of hormone-sensitive lipase (HSL).
    • Eicosapentaenoic acid (EPA) inhibits protein degradation by downregulating the ubiquitin-proteasome pathway and promotes lean body mass gain when combined with nutritional supplements.

    Conclusions:

    • Cancer cachexia is mediated by complex tumor and host factors affecting protein and lipid metabolism.
    • Eicosapentaenoic acid (EPA) shows promise in preventing muscle wasting and improving body composition in cancer cachexia.
    • Targeting the underlying mechanisms of cancer cachexia is crucial for effective therapeutic intervention.